NCF Member And Advisor Unearths New Truths About
ME/CFIDSBy Gail Kansky

[Parts of this article may be too complex for readers to understand. The
basic thing you should
know is that nearly all ME/CFIDS patients have a virus called HHV-6A and
inside that is a
retrovirus that one researcher has named the JHK virus. This has been known
and kept quiet as
we have continued to suffer for many years. Delaying publication serves
nobody but the
researcher in their quest to wrap up all tests for monetary purposes.-Ed]
As a speaker at the New Jersey CFS Association Inc. Eighth Annual CFS
Conference, Professor Alan Cocchetto, NCF board member and medical advisor,
broke open the truth about ME/CFIDS. It is not a truth that will lead to a
sigh
of relief, for ME/CFIDS is a severe and debilitating illness that is
devastating to
those who endure its wrath, but it is a truth that will lead to a better
understanding
and to treatments that are not just symptomatic. Hopefully, it will lead to
all getting well.
How did a patient and former engineering professor find out information
not
readily known by those researching ME/CFIDS? Professor Cocchetto explained,
"Most doctors are trained to look at medical journals but patents are a
goldmine of
information."
Anecdotally, human herpes virus 6, variant A (HHV-6A) accounts for about
80%
of those with ME/CFIDS, which is known to be both a multicausal and a
multisystemic illness. Another 20% have mycoplasma fementans/penentrans or
chlamydia pneumonia infections. Those with the latter two causal factors can
be
helped by antibiotic regimens which are offered by the NCF.
According to Dr. Lo of the Armed Forces Pathology Division, if you have a
mycoplasma infection too long, you are at increased risk for developing
cancer.
Therefore, we urge every patient to be tested for this. Mycoplasmas can now
be
tested for at Dr. Garth Nicolson's new commercial laboratory with your
insurance
footing the bill. The International Molecular Diagnostics, Inc. uses a DNA
analysis
technique called Forensic Polymerase Chain Reaction. [Call 714-799-7177.
Blood
tests are also available for sick pets.] Alas, the remainder of the patients
will not be
helped by antibiotics or will only be helped to a certain extent since the
chlamydia
or mycoplasmas are only secondary to the main causative agent....HHV-6A.
In the Annals of Internal Medicine's 1992 Lake Tahoe study that took
nearly a
decade to publish, 70% of Tahoe patients showed active HHV-6A infection, by
viral
culture assay, and testing was done in Dr. Robert Gallo's laboratory at the
National
Institutes of Health (NIH). (Ed. Note: Dr. Robert Gallo, as you recall, is
the
discoverer of AIDS.) MS patients have also shown a 70% HHV-6 infection rate
by
work done at the National Institute of Neurologic Diseases by Dr. Stephen
Jacobson. There are hundreds of papers that show that HHV-6A is the
accelerating
agent in AIDS. In fact, Professor Cocchetto says that "many researchers have
expressed to me that this (ME/CFIDS) resides somewhere between MS, cancer,
and AIDS."
In the U.S. government patent assigned to Dr. Robert Gallo and the
Department
of Health and Human Services (# 5,604,093 on 2/97), Dr. Gallo writes that
"The
presence of HBLV antibodies (Ed. note: HBLV is the former name of HHV-6A)
is elevated in the following disease groups:
Roseola (Exanthema subitum)
Burkitt's lymphoma
Hodgkin's disease
Mononucleosis-like syndromes
Sarcoidosis
Sjogren's Syndrome
A newly described infectious disease syndrome similar to that
seen in Lake
Tahoe characterized as an "acute mononucleosis-like syndrome" in adults,
commonly known as chronic fatigue syndrome (CFS). ALL (acute lymphocytic
leukemia) is diagnosed in children of Japanese, Caribbean, and African origin
and
HIV-1 antibody positive AIDS, ARC and PGL (persistent generalize
lymphadenopathy) patients."
Cocchetto explained that characteristics of HHV-6A include that HHV-6A is
in
the beta herpesvirus family and has a lipid envelope. This fact is
"important for
intervention," explained Professor Cocchetto, since the lipid envelope, not
the
virus, is much easier to attack when interceding in the virus. HHV-6A
shares 67%
homology with cytomegalovirus and the viral strain that ME/CFIDS has is the GS
strain, a strain that Dr. Gallo's group discovered from a patient with acute
lymphoblastic leukemia. While this does not mean that patients have
lymphoblastic
leukemia or that they will develop it, it can be hypothesized that this is a
smoldering
illness that eventually could possibly lead to an aberrant leukemia or
lymphoma.
HHV-6A can destroy CD4 and CD8 cells as well as Natural Killer (NK)
cells.
"Patients are losing CD8 counts at the rate of greater than or equal to 20%
per year
- a phenomenal loss!" exclaimed Professor Cocchetto. HHV-6A also contains
Marek's disease (lymphomas seen in chickens) and Adenovirus gene vectors.
"What the heck are these are doing in HHV-6A, we can only speculate and as
Dr.
Ablashi states, HHV-6A can increase EBV replication 5 to 10 fold."
Professor Cocchetto went on... "The key is that HHV-6A does something
that no
other herpes virus does. It has been reported by Dr. Torrisi, from Italy,
that it leaves
no viral glycoproteins (no marks to show it's been there) on the infected
cells!"
stated Cocchetto. By comparison, HIV has none of these capabilities.
Dr. Paul Levine has written in two different medical publications, that
among the
Tahoe outbreak patients, there was a reported increase in non-Hodgkin's
lymphoma
and brain cancer. Most horrific of all, the blood supply is not screened for
HHV-6A. Proclaimed Cocchetto, "For the National Institutes of Health or the
Center for Disease Control not to take this seriously and go after this with
some real
financial backing is unconscionable!" (Ed. note: Dr. Ablashi shared his
latest article
in the Journal of Clinical Virology (in press when this was written) where he
and his
colleagues conclude that "CFS patients must be acquiring Variant A HHV-6
infection in adulthood." This would indicate that HHV-6A is a primary
infection
and not a reactivation from childhood - thus not making this a ubiquitous
viral
infection as many have thought and reported!)
Dr. Thomas Bridge, in a patent for the US Government's DHHS (# 5,189,022
on
2/93), found that a "class of peptides which when administered to patients not
infected with HIV, but having CFS. reduce fatigue, tension, anger, confusion
and
improve cognitive and neuromotor performance...In recent work, protein kinase
A
activity in humans has been shown to be increased by Peptide-T...the principal
immunologic test in this study was the PCR signal for HHV-6....It appears that
Peptide-T, a protein kinase A enhancer, produces both symptomatic and
functional
improvement in patients with a diagnosis of Chronic Fatigue Syndrome. It
accomplishes this improvement without changing the underlying viral
infection."
[Ed. note: See related story on Peptide-T and other treatments.]
Retroviral Evidence Seen In CFS:
Dr. William Carter, of Hemispherx Biopharma (# 5,958,718 on 9/99) when
writing about virologic studies, wrote "I have also observed that the
majority of
these patients are infected with herpes-6...I have also found EB
(Epstein-Barr)
virus in many of these patients as well as a novel retrovirus similar (though
different genetically) to HIV, a retrovirus causing acquired immune
deficiency or
AIDs. Specimens from several patients I have studied indicate the intriguing
possibility of 'pseudotyping' as a means of spreading this disease. By
pseudotyping, I refer, for example, to the coat of a herpes type 6 virus
surrounding the genetic material for a retrovirus. This would give rise to a
novel
form of contagion where the infectious agent spreads epidemiologically through
the population like a herpes virus but the genetic information being spread is
actually that of a retrovirus...leading ultimately to mental deterioration and
morbidity."
In an earlier patent, Dr. Sidney Grossberg, a world renown virologist
from the
Medical College of Wisconsin, wrote (# 5,827,750 on 10/98) "The human virus
on which the present invention is based has not been classified as to which
virus
family it belongs, but it most nearly resembles a retrovirus ....The present
invention relates to the detection of the presence of an NMA (neuromyasthnia)
virus that is associated with CFIDS." He goes on to talk of the "protein
spikes in
the envelope" which are called peplomers and these spikes are characteristic
of a
retrovirus. He calls this retrovirus the "JHK virus." He mentions that the
retrovirus that is close to the same size is called the "mouse mammary tumor
virus." In his only publication on the virus, one that went unannounced by
the
CFIDS Association despite their funding of him, Grossberg writes ( Res Virol,
1997; 148(3): 191-206 ), "The human B-lymphoblastoid cell line, designated
JHK-3, with pre-B-cell characteristics, chronically produces two viruses,
Epstein-Barr virus (EBV) and JHK virus, an apparently novel retrovirus...most
nearly resembling C-type retroviruses." Professor Cocchetto admitted that the
driving force behind uncovering this research was reading Hillary Johnson's
Osler's Web: Inside the Labyrinth of Chronic Fatigue Syndrome. In fact, he
shared this quote from the book by Dr. Sidney Grossberg, "We may have a
genetic recombination of herpes and retrovirus here." [ Ed. note: Perhaps the
intriguing full truth given in Ms. Johnson's epic book was the very reason
that
the CAA gave it such a poor review.]
Was this information just coming from the United States? Certainly not!
From Denmark, Dr. Mette Summerlund wrote on a "Type C-like human
retrovirus linked to Multiple Sclerosis" and used the same language calling it
"double infected with EBV and a hitherto uncharacterized human retrovirus..."
Dr Michael Holmes, from New Zealand, a name most in the CFS arena
recognize, wrote in The Clinical and Scientific Basis for Myalgic
Enchelphalomyelitis/Chronic Fatigue Syndrome (1/97) that "structures
consistent in size, shape and character with various stages of a Lentivirus
(retrovirus) replicative cycle were observed by electron microscopy in
cultures
from CFS patients..."
In 1995, Dr. Jay Levy, a world famous virologist from University of
California, wrote on the "Isolation of Infectious Agent for CFS: Innoculation
of
Animals," from one of his patents, that he used cultures that were "evaluated
for
reverse transcriptase activity" and "we have found that the CD11b+ cells
(suppressor CD8+ cells) decrease during CFS."
Going back to 1991, Dr. Elaine DeFreitas, before the CFIDS Association of
America cut her funding and her research off, wrote that "These data support
an
association between an HTLV-II like virus and CFIDS."
We can even go back to 1959 when Dr. Bjorn Sigudsson, from the Institute
for Experimental Pathology in Iceland, wrote on Icelandic Disease, now known
as CFS (ME). "This incredibly intelligent soul," said Professor Cocchetto,
conceived the concept that slow viral infections, in particular, the visna
(sheep)
virus, could take a long time to do its damage before it could be seen.
As he lay dying, he dictated to a colleague the similarities between visna (a
retrovirus) and multiple sclerosis.
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